The present study aimed to investigate the role of microRNA (miR)-101 in acute lymphoblastic leukemia progression and chemoresistance. Furthermore， a novel target gene of miR-101 was identified. Here， we confirmed that miR-101 was significantly downregulated in the blood samples of patients with T-cell acute lymphoblastic leukemia (T-ALL) compared with the healthy controls， as determined by reverse transcription quantitative polymerase chain reaction (RTqPCR) analysis. The in vitro experiments demonstrated that miR-101 significantly repressed the proliferation and invasion， and induced potent apoptosis in Jurkat cells， as determined by CCK-8， flow cytometer and cell invasion assays. Luciferase assa... More
The present study aimed to investigate the role of microRNA (miR)-101 in acute lymphoblastic leukemia progression and chemoresistance. Furthermore， a novel target gene of miR-101 was identified. Here， we confirmed that miR-101 was significantly downregulated in the blood samples of patients with T-cell acute lymphoblastic leukemia (T-ALL) compared with the healthy controls， as determined by reverse transcription quantitative polymerase chain reaction (RTqPCR) analysis. The in vitro experiments demonstrated that miR-101 significantly repressed the proliferation and invasion， and induced potent apoptosis in Jurkat cells， as determined by CCK-8， flow cytometer and cell invasion assays. Luciferase assay confirmed that Notch1 was a target gene of miR-101， and western blotting showed that miR-101 suppressed the expression of Notch1 at the protein level. Moreover， functional restoration assays revealed that Notch1 mediates the effects of miR-101 on Jurkat cell proliferation， apoptosis and invasion. miR-101 enhanced the sensitivity of Jurkat cells to the chemotherapeutic agent adriamycin. Taken together， our results show for the first time that miR-101 acts as a tumor suppressor in T-cell acute lymphoblastic leukaemia and it could enhance chemotherapeutic sensitivity. Furthermore， Notch1 was identified to be a novel target of miR-101. This study indicates that miR-101 may represent a potential therapeutic target for T-cell acute lymphoblastic leukemia intervention.
